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Qualitative and quantitative immunoglobulin production by specific bacteria in chronic tonsillar disease
Author(s) -
Koch R. James,
Brodsky Linda
Publication year - 1995
Publication title -
the laryngoscope
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.181
H-Index - 148
eISSN - 1531-4995
pISSN - 0023-852X
DOI - 10.1288/00005537-199501000-00011
Subject(s) - immunology , antibody , immunoglobulin e , immunoglobulin g , immunoglobulin m , immunoglobulin a , haemophilus influenzae , tonsillitis , medicine , biology , microbiology and biotechnology , pathology , antibiotics
Tonsillar tissue lymphocyte (TTL) function as measured by immunoglobulin production was assessed in vitro in 60 tonsils, 51 diseased and 9 normal controls. The diseased specimens were from children (aged 3 to 10 years) clinically classified as having recurrent tonsillitis (RT), idiopathic tonsillar hyperplasia (ITH), or recurrent tonsillitis with hyperplasia (RT/H). TTLs were challenged with intact, heat‐inactivated bacteria found in the core of diseased tonsils— Streptococcus pyogenes (SP) and Haemophilus influenzae type B (HIB) as well as the dominant bacterium (DB) grown from that particular tonsillar core. The phytomitogen, leukoagglutinin (LA), was used as a nonspecific activator. Qualitative immunoglobulin production was assessed for the immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) classes. Immunoglobulin‐specific production was quantified at the basal level, and at 2, 4, and 6 days following stimulation. Stimulation with HIB produced the greatest amount of IgG and IgM in TTLs from control tonsils. The DB was a relatively weak stimulator of normal (control) TTLs, yet produced relatively brisk IgG responses in the RT and ITH categories. It did, however, yield only marginal IgM secretion in these groups. IgA was consistently produced after stimulation in diseased TTLs, yet was not elicited from normal TTLs. The aforementioned findings suggest a differential qualitative and quantitative immunoglobulin response for healthy, recurrently infected, and hyperplastic tonsils. Lymphocyte hypofunction along with structural changes associated with hyperplasia may be central to the etiology of chronic tonsillar disease. The tonsillar immunologic response in disease and health is discussed.